The overall objective of the present study is to investigate the mechanism(s) by which gonadotropins regulate ovarian function. The following conclusions were drawn from the studies carried out during the present grant period, 1) cyclic AMP exists in bound and free forms in the ovarian tissue. Approximately 60 per cent of the cyclic AMP binding sites are endogenously occupied. hCG and LH treatment fully saturated the remaining binding sites. The newly synthesized cyclic AMP is compartmentalized in the ovary and the whole amount is not available for activation. 2) Cyclic AMP is an obligatory intermediate in gonadotropin stimulated steroidogenesis. The lack of cyclic AMP accumulation in response to low doses of hCG or LH is due to rapid degradation of cyclic AMP by phosphodiesterases. 3) hCG and LH injection causes a reducation in the ovarian LH/hCG receptors and this inhibition (desensitization) results in inhibition of further metabolic activities coupled to the hormone-receptor. 4) Although cholera toxin (an agent known to stimulate cyclic AMP accumulation in most tissue) stimulates ovarian steroidogenesis in the ovary, the receptor for cholera toxin appears to be quite distinct from gonadotropin receptor. This is based upon the observation that gangliosides (binder for cholera toxin) do not compete with hCG or LH for stimulating steroidogenesis.